同济大学发表最新Cell子刊论文

Core Viewpoint - The study reveals that Itaconate, contrary to its traditional anti-inflammatory perception, promotes inflammatory responses in tissue-resident alveolar macrophages, exacerbating acute lung injury [2][9]. Group 1: Effects of Itaconate - Itaconate enhances the production of pro-inflammatory cytokines and activates the NLRP3 inflammasome in alveolar macrophages [4][7]. - Pre-treatment with Itaconate worsens LPS-induced lung tissue damage, while knocking out ACOD1 significantly improves survival rates in acute lung injury mouse models [2][6]. Group 2: Comparison with Bone Marrow-Derived Macrophages - The response of bone marrow-derived macrophages (BMDM) to Itaconate is opposite to that of tissue-resident alveolar macrophages, indicating the critical role of the pulmonary microenvironment in shaping macrophage immune metabolism [5][10]. Group 3: Itaconate Derivatives - Unlike natural Itaconate, its derivatives, dimethyl itaconate (DI) and 4-octyl itaconate (4OI), can inhibit the inflammatory response in alveolar macrophages [4][7]. Group 4: Implications for Clinical Treatment - The findings suggest that further research is necessary before considering Itaconate for clinical applications in treating inflammatory diseases, given its unexpected pro-inflammatory role in tissue-resident alveolar macrophages [9][10].